Interleukin-11 increases cell motility and up-regulates intercellular adhesion molecule-1 expression in human chondrosarcoma cells

J Cell Biochem. 2012 Nov;113(11):3353-62. doi: 10.1002/jcb.24211.

Abstract

Interleukin-11 (IL-11) was originally identified as the cytokine that could induce the proliferation of human cells. Recent studies have shown that IL-11 plays a critical role in tumor growth, angiogenesis, and metastasis. Chondrosarcoma is a type of highly malignant tumor with a potent capacity to invade locally and cause distant metastasis. However, the effects of IL-11 on human chondrosarcoma cells are largely unknown. Here, we found that IL-11 increased the migration and expression of intercellular adhesion molecule-1 (ICAM)-1 in human chondrosarcoma cells. We also found that human chondrosarcoma tissues had significant expression of the IL-11 which was higher than that in primary chondrocytes. The phosphatidylinositol 3-kinase (PI3K), Akt, and NF-κB pathways were activated by IL-11 treatment, and the IL-11-induced expression of ICAM-1 and migration activity were inhibited by the specific inhibitors and mutant forms of PI3K, Akt, and NF-κB cascades. Taken together, our results indicate that IL-11 enhanced the migration of the chondrosarcoma cells by increasing ICAM-1 expression through the IL-11Rα receptor, PI3K, Akt, and NF-κB signal transduction pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bone Neoplasms / genetics
  • Bone Neoplasms / metabolism*
  • Bone Neoplasms / pathology
  • Case-Control Studies
  • Cell Movement / drug effects
  • Chondrocytes / cytology
  • Chondrocytes / metabolism
  • Chondrosarcoma / genetics
  • Chondrosarcoma / metabolism*
  • Chondrosarcoma / pathology
  • Enzyme Inhibitors / pharmacology
  • Humans
  • Intercellular Adhesion Molecule-1 / genetics
  • Intercellular Adhesion Molecule-1 / metabolism*
  • Interleukin-11 / antagonists & inhibitors
  • Interleukin-11 / genetics*
  • Interleukin-11 Receptor alpha Subunit / genetics
  • Interleukin-11 Receptor alpha Subunit / metabolism
  • NF-kappa B / genetics
  • NF-kappa B / metabolism
  • Phosphatidylinositol 3-Kinase / genetics
  • Phosphatidylinositol 3-Kinase / metabolism
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism
  • RNA, Small Interfering / genetics
  • Signal Transduction / drug effects
  • Tumor Cells, Cultured
  • Up-Regulation / drug effects

Substances

  • Enzyme Inhibitors
  • Interleukin-11
  • Interleukin-11 Receptor alpha Subunit
  • NF-kappa B
  • RNA, Small Interfering
  • Intercellular Adhesion Molecule-1
  • Phosphatidylinositol 3-Kinase
  • Proto-Oncogene Proteins c-akt